Published online Sep 15, 2024. doi: 10.4239/wjd.v15.i9.1916
Revised: June 4, 2024
Accepted: July 2, 2024
Published online: September 15, 2024
Processing time: 174 Days and 4 Hours
Diabetic nephropathy (DN) is the most frequent chronic microvascular conse
To explore the protective effect of Cor against podocyte injury in DN mice and the underlying mechanisms.
Streptozotocin and a high-fat diet were combined to generate DN mice models, which were then divided into either a Cor group or a DN group (n = 8 in each group). Mice in the Cor group were intraperitoneally injected with Cor (30 mg/kg/d) for 12 wk, and mice in the DN group were treated with saline. Bio
Compared with the control group, the DN mice models had increased fasting blood glucose, glycosylated hemoglobin, triglycerides, and total cholesterol, decreased nephrin and podocin expression, increased apoptosis rate, elevated inflammatory cytokines, and enhanced oxidative stress. All of the conditions mentioned above were alleviated after intervention with Cor. In addition, Cor therapy improved SIRT1 and AMPK expression (P < 0.001), inhibited reactive oxygen species and oxidative stress, and elevated autophagy in HG-induced podocytes (P < 0.01).
Cor alleviates podocyte injury by regulating autophagy via the SIRT1-AMPK pathway, thereby exerting its protective impact on renal function in DN mice.
Core Tip: This study explored the protective effects of Corilagin (Cor) against podocyte injury in diabetic nephropathy (DN). Cor treatment markedly attenuated fasting blood glucose, glycosylated hemoglobin, triglycerides, and total cholesterol, increased nephrin and podocin expression, reduced apoptosis rate, and inhibited inflammatory cytokines and oxidative stress. In addition, Cor contributed to improving SIRT1 and AMPK expression, inhibited reactive oxygen species and oxidative stress, and elevated autophagy in high-glucose-treated podocytes. Thus, Cor might be a potential therapeutic agent for the treatment and clinical management of DN.